Neurological disease in ruminants Flashcards
What parts of the neuro assesment can be performed in ruminants?
- General - Mentation and behaviour
- head/neck/face - Head position and co-ordination, Cranial nerve reflexes
- limb - Limb position and co-ordination
- Trunk - Gait analysis, Muscle tone, Body position, Panniculus (cutaneous trunci) reflex
- Tail/perineum/anus - Tail tone, Perineal and anal reflexes
- All - Sensation
What propreoceptive assessments can be perfomred in ruminants?
- Conscious proprioceptive positioning (knuckling test) - sheep, goats, calves
- Wheelbarrow - sheep, gaots, calves (care with rumen pressure on diaphragm
- Gait analysis
- Standing position
- Hoof inspection
What is the approach to a farm animal neurological case?
- History and clinical exam
* Assess primary or secondary
* Localisation of lesion –> narrows ddx list - Further diagnostics to confirm suspected diagnosis
* Bloods (biochem/haematology)
* CSF tap
* Post-mortem - Treatment
* Often based on presumptive diagnosis
* May confirm/rule out diagnosis (treatment trial)
What are the different parts of the neurological exam in ruminants?
step one of neuro assessment is workign out if the disease is primary or secondary:
how do you work out if a neuro disease is primary of secondary?
History and clinical exam
Primary
- Conditions directly affecting the neurological system (e.g. brain abscesses, spinal cord injuries)
Secondary
- Conditions that present with neurological signs but are not of neurological origin (e.g. hypomagnesaemia, twin lamb disease)
What is step two locating a neuro lesion?
Is the lesion rostral or caudal to foramen magnum?
e.g. is the brain affected or not?
Step 3 of locating a neuro lesion is : Further localising the lesion, What does this involve?
once you have worked out if the brain is affected you can then work out what the area affected is by workign out which part of the body is affected and therefor ethe likely structure affected
If there are whole body signs then you can use these clinical signs to work out where the lesion is
How do you localise a peripheral lesion?
- Abnormalities of peripheral nerve branches result in presentations opposing to the nerve’s motor function that affect innervated muscle
- If flexor muscles are innervated, injury will present as hyperextension
- If extensor muscles are innervated, injury will present as flexion
- If the affected branch is sensory, sensation of the innervated area will also be affected
- Can still locate the lesion to the main spinal nerve (from which the nerve has branched) using table on previous slide
What additional diagnostic tools can be used to aid with neuro disease diagnosis?
how is this obtained?
cerebrospinal fluid:
* Aids diagnosis –> rarely diagnostic on its own
* Obtain from midpoint of lumbosacral space (cattle/goats = L6, sheep L6 or L7)
* Depression on midline between last palpable lumbar and 1st palpable sacral vertebrae
* Standing animal (if recumbent place in sternal with hindlimbs forward)
* Adult cattle = 4” spinal needle
* Calves & adult small ruminants = 2” hypodermic needle
* Lambs and kids = 1” hypodermic needle
- Clip and surgical prep
- Local anaesthesia –> bleb of procaine
- Sedate if needed
- Collect 1-3ml of CSF –> carefully draw back syringe to minimise trauma
- Collect EDTA sample and plain sample
When can biochem and haem be used for neuro disease diagnosis?
Can be of use if secondary neurological conditions suspected
* Magnesium
* Calcium
* Sodium
* Acid-base balance
* Specific assays (e.g. toxins)
*
What further tests can be done on CSF fluid to aid neuro disease diagnosis?
Additional tests can be performed as required although rarely done
e.g. electrolytes, glucose, biochemical parameters
Culture
* Send to external lab
* Varying results
* Listeria = typically difficult to culture
* Septic meningitis = typically cultures well
What are the common aetiologies for ruminant neurological conditions?
- metabolic, malformation
- infectious, inflammatory, immune-mediated, iatrogenic, idiopathic, inheritied
- trauma, toxic
What are 2 most common cerebral conditions in calves?
What are 2 less common cerebral conditions of calves?
**Most common cerebral conditions in calves: **
* Cerebral corticonecrosis (CCN)
* Septic meningitis
Less common cerebral conditions of calves:
* Hypernatremia (salt toxicity)
* Brain abscesses
metabolic
What are two secondary neurological conditions related to negative energy balance?
Why does this happen?
Nervous ketosis (cattle)/pregnancy toxaemia (sheep)
Increased ketones and decreased glucose = negative effects on brain function
Why does pregancy toxaemia in sheep occur?
- Energy demands of foetus(es) in late gestation > energy obtained from diet
- Often associated with temporary food deprivation or reduction in intakes
- Primarily seen in ewes carrying twins/triplets in more intensive systems during last 2 weeks of gestation
What are the clinical signs of pregnancy toxaemia in sheep?
Early stages
* Separation from group
* Apparent blindness
* Sheep seem alert but do not want to move (even if dog present)
* Bump into obstacles and exhibit head pressing
Later stages
* Marked drowsiness
* Facial twitching, jaw champing, salivation
* Deviations of head position
* Star-gazing and ataxia
* Seizures
* Marked drowsiness seen between seizures
* Ketone breath
Final stages
* Recumbency develops after 3-4 days
* Develops comatose state
* Typically lasts for 3-4days
* If foetal death occurs, ewe appears to recover but secondary toxaemia results in deterioration and death
What is the treatment for pregnancy toxaemia in sheep?
- Parenteral glucose
- 5-7g glucose IV 6-8x daily recommended
- Supportive IV fluids
- Hartmann’s or saline
- Oral propylene glycol
- 100mL once daily
- In milder cases can be very effective alone
- Supplement with calcium and potassium
- Increases success rate
- Can consider inducing lambs if in early stages of disease
- If do not think ewe will survive the delay between induction and parturition (24hrs) C-sec can be considered
What is the prevention and control for pregnancy toxaemia in sheep?
- When clinical cases occur carefully monitor rest of flock and treat affected animals immediately with oral glucose/propylene glycol/glycerol
- Prevent by ensuring there is a rising plane of nutrition in 2nd half of pregnancy
- Nutrition needs to be improving
- May need to restrict in early pregnancy to achieve this
- Recommend scanning and feeding singles/twins/triplets separately if possible
metabolic
What it the cause of nervous ketosis in cattle?
What are the clinical signs?
Uncommon presentation of ketosis
* Likely due to isopropanol –> breakdown product of acetone
* Hypoglycaemia also likely to contribute
* Ketone bodies further exacerbate signs
Sudden onset neurological signs occurring in short recurring bouts:
* Circling and aimless wandering
* Crossing limbs and ataxia
* Apparent blindness, walking into objects (including people), head pressing
* Hyperaesthesia
* Mild tremors
Key ddx is BSE –> notifiable and of VPH importance (if high ketones then ok, but if normal ketones then ring defra)
How is nervous ketosis diagnosed and treated?
- Diagnosis based on clinical signs together with blood BHB concentration > 3.0 mmol/L
Treatment:
* IV glucose (500ml of 50% solution)
* Rapid improvement but is transient (only lasts 3-4hrs)
* Oral propylene glycol
* 300ml once daily for 5 days
* Glucocorticoids
* Best responses if given with glucose
* Probably due to glucose repartitioning – previously thought to be gluconeogenesis
* Limited evidence basis for treating less severe cases of ketosis
Control- Key to control is transition management
metabolic/nutritional:
What are the causes of Cerebrocortical necrosis (CCN) (Polioencephalomalacia)?
Thiamine (Vit B1) deficiency/inadequacy
* High concentration of thiaminases formed in rumen (reasons unknown)
* Destroy thiamine (produced by microbes)
* Increased pyruvate (thiamine important component of metabolic enzymes)
* Negative effect on glucose pathways damage to cerebral neurons
Sulphur induced CCN
uncommon at the moment but might occur again
* Diets high in sulphates
* Young cattle on feedlots (6-18mths old)
What is the clincial presentation of Cerebrocortical necrosis (CCN)?
- Usually young, growing animals –> weaned lambs and calves most often
- Typically a history of recent dietary change (about 2 weeks prior)
- Disruption of rumen microflora
- Clinical signs start with sudden onset blindness, aimless wandering and circling, head pressing, star-gazing
- Progress over 12-24hrs to lateral recumbency and opisthotonos
- Death occurs in a few days in untreated animals
How is Cerebrocortical necrosis (CCN) diagnosed?
- History and clinical exam
- Differential diagnosis = other cerebral conditions
- Meningitis
- Lead poisoning
- Twin lamb disease/nervous ketosis
- Vitamin A deficiency
- Ante-mortem definitive diagnosis not possible
- Response to thiamine treatment = highly suggestive
- Sulphur induced CCN does not respond to thiamine treatment
- Diagnosis confirmed on post-mortem exam
- Brain fluoresces under UV light
What is the treatment and control of Cerebrocortical necrosis (CCN)?
**Thiamine (vit B1) treatment **– 10mg/kg
* Give (slow) IV initially
* Repeat every 3hrs up to 5 doses – can be IV or IM
* Prognosis is good if treatment instigated early
* Use B1 products – multivitamins often do not have high enough B1 for treatment
* Supportive care. May also need dexamethasone (1mg/kg) if cerebral oedema
Supplementation of diets with thiamine for ongoing control
* 3mg/kg dry matter (may need to be higher on some farms)
* Ensure roughage in diet
* Ensure sulphur content of diet is appropriate
metabolic
What are the two forms of hypomagnesaemia?
What do you need to be worried about?
Pathogenesis covered in down cow lecture
Common in cattle, occurs rarely in sheep
Low serum magnesium - Alterations in nerve impulses to muscles
* Acute form –> hyperaesthesia, ataxia, collapse, seizures
* Subacute form –> wild facial expression, hypermetric gait, muscle tremors, spasmodic urination and defecation
* May present as sudden death - Important ddx is anthrax (notifiable) - if evidence of seizure then less likely to be anthrax
How is hypomagnesaemia diagnosed?
- Diagnosis based on characteristic clinical signs and history
- Typically seen in cows at pasture in Spring/Autumn with older suckling calves at foot
- Lots of milk demand –> increased magnesium losses
- Young, growing grass has lower magnesium content –> reduced magnesium consumption
- Live animal = blood sample
- Lithium heparin (green top) tube
- External lab or in house analyser
- Worth also testing for calcium and phosphorus at same time
- Dead animal =** vitreous humor**
- Remains stable after death longer than serum/plasma concentration
- Use 14G or 16G needle and aspirate with syringe
- Do not sample aqueous humor – easily contaminated by iris tissue if deteriorating
What is the treatment of hypomagnesaemia?
- Emergency!
- Sedate if seizuring
- IV calcium with magnesium added
- SC magnesium
DO NOT GIVE WHOLE BOTTLE OF MAGNESIUM IV!!
black bottle of Mg is only for SC (or a little bit IV)
What is the prevention and control of hypomagnesaemia?
- Supplement diet with magnesium
- Included in TMR or concentrates –> typically for dairy cows
- Magnesium salts (daily oral drench, top dressing pasture, water, licks)
- Graze suckled cows on lower risk pastures
- Consider calving earlier in winter/late autumn so cows are housed until calves are weaned
- Often not practical
What does copper deficiency of ewews/does in mid pregnancy do?
Why can you not diagnose on blood copper?
What is the treatment
Sway back:
* Congenital cerebrospinal swayback - Lambs born dead or weak and unable to stand
* Progressive spinal swayback - Stiff staggering gait, hindlimb ataxia
* Cerebral oedema - Reported in Wales only
** Diagnosis** - Blood copper not reflective of copper status because copper stored in the liver - Liver biopsy is a better indicator
* Interpret results with care because animals may show clinical signs before liver/blood copper concentration very low
- Treatment involves oral supplementation of copper
Severely affected lambs = poor prognosis - Prevention is better
Care due to susceptibility of copper tox
What are the two types of Vitamin A deficiency (hypovitaminosis A)?
What are the main clinical signs?
What is the treatment and prevention?
**Primary deficiency **–> associated with diets insufficient in vitamin A
Secondary deficiency –> associated with chronic liver or enteric disease
Failure of conversion of carotene to vit A
Main clinical signs:
* Night blindness – earliest c/sign –> young adult animals
* Corneal keratinisation, mucoid ocular discharge, photophobia
* Skeletal muscle paralysis (weakness and ataxia that starts in hindlimbs) –> young animals
Treatment Vitamin A supplementation at 440 IU/kg (10-20x maintenance requirement)
Response to treatment is rapid
Prevention:
Ensure adequate dietary vitamin A
40IU/kg is minimum daily requirement for all species
